The autonomic nervous system includes sympathetic and parasympathetic pathways. Stimulation of nerves in these pathways can affect cardiac operation or function. In general, sympathetic activation causes an increase in heart rate and inotropy (contractility) and hence cardiac output. Frantz, “Beta blockade in patients with congestive heart failure,” Postgraduate Medicine, 108(3), 103–118 (2000), explains that “[i]n a teleological sense, an acute increase in sympathetic drive was advantageous for our ancestors. When they were being pursued by a tiger or bleeding from a wound, increasing heart rate, peripheral tone, and myocardial contractility allowed them to reach safety or maintain central perfusion.” In contrast, parasympathetic activation generally causes a decrease in atrial rate and contractile force, atrio-ventricular nodal conduction, and ventricular contractile force. Hence, selective activation or stimulation of the autonomic nerves can provide a means for cardiac control. While reports of autonomic nerve stimulation are known, a need exists for setting stimulation parameters (e.g., power level, thresholds, etc.), especially when stimulation occurs via an implantable device with a limited power supply.